DSpace Arşivi :: by Yazar "Ciftci, Osman" değerine göre listeleniyor

Yazar "Ciftci, Osman" seçeneğine göre listele

Listeleniyor 1 - 20 / 72

18?-glycyrrhetinic acid attenuates global cerebral ischemia/reperfusion-induced cardiac damage in C57BL/J6 mice
(Univ Sao Paulo, Conjunto Quimicas, 2022) Turkmen, Nese Basak; Yuce, Hande; Taslidere, Asli; Sahin, Yasemin; Ayhan, Idris; Unuvar, Songuel; Ciftci, Osman
The aim of the present study is to investigate the cardioprotective effects of 1813-glycyrrhetinic acid (1813-GA) against oxidative and histological damage caused by global cerebral ischemia/ reperfusion (I/R) in C57BL/J6 mice. All male mice (n:40) were randomly divided into four groups: (1) sham-operated (Sham), (2) I/R, (3) 1813-GA, and (4) 1813-GA+I/R. Ischemia was not applied to the sham and 1813-GA groups. In the I/R group, the bilateral carotid arteries were clipped for 15 min to induce ischemia, and the mice were treated with the vehicle for 10 days. In the 1813-GA group, the mice were given 1813-GA (100 mg/kg) for 10 days following a median incision without carotid occlusion. In the 1813-GA+I/R group, the ischemic procedure performed to the I/R model was applied to the animals and afterwards they were intraperitoneally (i.p.) treated with 1813-GA (100 mg/kg) for 10 days. It was found that global cerebral I/R increased TBARS levels and decreased antioxidant parameters. The 1813-GA treatment decreased the level of TBARS and increased GSH, GPx, CAT, SOD activities. Also, the control group cardiac tissue samples were observed to have a normal histological appearance with the Hematoxylin-Eosin staining method. Histopathological damage was observed in the heart tissue samples belonging to the I/R group. The 1813-GA treatment ameliorates oxidative and histological injury in the heart tissue after global ischemia reperfusion, and may be a beneficial alternative treatment.
Ameliorating effects of quercetin and chrysin on 2,3,7,8-tetrachlorodibenzo-p-dioxin-induced nephrotoxicity in rats
(Sage Publications Inc, 2012) Ciftci, Osman; Ozdemir, Ilknur; Vardi, Nigar; Beytur, Ali; Oguz, Fatih
The aim of this study is to investigate the beneficial effects of the quercetin (Q) and chrysin (CH) against nephrotoxicity induced by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), a persistent environmental contaminant, in rats. Rats were divided randomly into six equal groups. TCDD, Q and CH were administered by gavages dissolved in corn oil at the doses of 2 mu g/kg/week, 20 mg/kg/day and 50 mg/kg/day, respectively. The kidney samples were taken from all rats on day 60 for the determination of thiobarbituric acid reactive substances (TBARS), glutathione (GSH), catalase (CAT), glutathione peroxidase (GPx) and superoxide dismutase (SOD) levels by spectrophotometric method. The results indicated that TCDD significantly induced lipid peroxidation and reduced antioxidant activities in rats. In contrast, Q and CH significantly prevented toxic effects of TCDD via increased GSH, CAT, GPx and SOD levels but decreased formation of TBARS. Also, it was determined that exposure to TCDD leads to significant histological damage in kidney tissue, and these effects can be eliminated with Q and CH treatment. In conclusion, the current study showed that exposure to TCDD can exert nephrotoxicity in rats. When Q and CH were given together with TCDD, they prevented nephrotoxic effects of TCDD. Their preventive effect lends more support to the role of oxidative and histological damage in the overall toxicity of TCDD.
Amine-fnctionalized silver and gold N-heterocyclic carbene complexes: Synthesis, characterization and antitumor properties
(Elsevier Science Sa, 2019) Kizrak, Umran; Ciftci, Osman; Ozdemir, Ilknur; Gurbuz, Nevin; Dusunceli, Serpil Demir; Kaloglu, Murat; Mansour, Lamjed
Diisopropilamine-tethered benzimidazolium salts have been prepared as precursors for Ag(I)-NHC and Au(I)-NHC complexes. These NHC ligands were metallated with Ag2O on moderate conditions to give novel silver-NHC complexes. Gold-NHC complexes have been obtained by transmetalation using the silver-NHC precursor. The structures of all compounds were characterized by H-1 NMR, C-13 NMR, IR and elemental analysis techniques. The cytotoxic properties of the silver(I) and gold(I) complexes have been assessed in various human cancer lines, including cisplatin-sensitive and resistant cell. IC50 values of these four complexes were determined by the MTS based assay on three human cancer cell lines (SHSY5Y, HTC116 and HEP3B) and human healthy cell line (HF). These silver and gold N-heterocyclic carbene complexes have been highlighted metal-based cancer therapeutic agent with unique structures and functions. These strategies provide exciting opportunities for discovering new type metalodrug. (C) 2019 Elsevier B.V. All rights reserved.
Anti-inflammatory Montelukast prevents toxic effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin: Oxidative stress, histological alterations in liver, and serum cytokine levels
(Sage Publications Inc, 2016) Bentli, Recep; Ciftci, Osman; Cetin, Asli; Otlu, Ali
This study aimed to investigate the potential beneficial effects of the montelukast (ML) on oxidative stress and histological alterations in liver tissues and cytokine levels in rats intoxicated with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Rats were divided randomly into four equal groups (control, TCDD, ML, TCDD + ML). TCDD were administered by gavages dissolved in corn oil at the doses of 2 mu g/kg/week, and ML was given intraperitoneally at the dose of 10 mg/kg/day. Oxidative status, histological alterations, and cytokine levels were analyzed on day 60. The results showed that although TCDD induced oxidative stress via significant increase in formation of thiobarbituric acid reactive substance, it caused a significant decline in glutathione (GSH), catalase (CAT), and superoxide dismutase (SOD) levels in liver. Besides, TCDD led to significant histopathological damage in liver and serum cytokine levels alterations (increase in tumor necrosis factor alpha and interleukin 1 beta levels). In contrast, ML treatment reversed oxidative effects of TCDD by increasing the levels of GSH, CAT, and SOD and decreasing the formation of TBARS. Also, it can normalize the levels of histological and cytokine alterations induced by TCDD. In conclusion, it was determined that TCDD exposure caused adverse effects on cytokine levels, histological alterations, and oxidative stress in rats. However, ML treatment partially eliminated toxic effects of TCDD. Thus, it was judged that coadministration of ML with TCDD may be useful to attenuate the negative effects of TCDD.
Antioxidant Effect of Ethanolic Extract of Propolis in Liver of L-NAME Treated Rats
(Wroclaw Medical Univ, 2015) Selamoglu, Zeliha S.; Ozdemir, Ilknur; Ciftci, Osman; Gulhan, Mehmet F.; Savci, Ahmet
Background. The blocking of nitric oxide synthase (NOS) activity may cause vasoconstriction with formation of reactive oxygen species. Propolis is a natural product collected from plants by honeybees. Propolis has biological and pharmacological properties. Objectives. This study was designed to investigate the effects of propolis on catalase (CAT) activity, nitric oxide (NO) and malondialdehyde (MDA) levels in the liver tissues of NOS inhibited rats by N omega-Nitro-L-arginine methyl ester (L-NAME). Material and Methods. Rats were given a NOS inhibitor (L-NAME, 40 mg/kg, intraperitoneally) for 15 days to provoke hypertension and propolis (200 mg/kg, by gavage) the last 5 of the 15 days. Results. Nitric oxide levels in the liver tissue of the rats given L-NAME significantly decreased (p < 0.01). That parameter did not significantly alter in the liver of rats treated with propolis compared to the control group. CAT activity and MDA levels in the liver of the rats administrated L-NAME significantly increased compared to the control group (p < 0.01). These parameters significantly decreased in the liver of the rats given L-NAME + propolis compared to the L-NAME group (p < 0.01). Conclusions. The present data shows that L-NAME in the liver may enhance oxidative stress via inhibited nitric oxide synthase. Our results also suggest that this effect is suppressed by the antioxidant properties of propolis in the liver tissue of NOS inhibited rats
Antioxidative effects of curcumin, ?-myrcene and 1,8-cineole against 2,3,7,8-tetrachlorodibenzo-p-dioxin-induced oxidative stress in rats liver
(Sage Publications Inc, 2011) Ciftci, Osman; Ozdemir, Ilknur; Tanyildizi, Sadettin; Yildiz, Sedat; Oguzturk, Hakan
The aim of this study was to investigate the effectiveness of curcumin, beta-myrcene (myrcene) and 1,8-cineole (cineole) on antioxidant defense system in rats given a persistent environmental pollutant (2,3,7,8-tetrachlorodibenzo-p-dioxin, TCDD). Rats (n = 112) were divided randomly into 8 equal groups. One group was kept as control and given corn oil as carrier. TCDD was orally administered at the dose of 2 mu g/kg/week. Curcumin, myrcene and cineole were orally administered at the doses of 100 mg/kg/day, 200 mg/kg/day and 100 mg/kg/day, respectively, by gavages dissolved in corn oil with and without TCDD. The liver samples were taken from half of all rats on day 30 and from the remaining half on day 60 for the determination of thiobarbituric acid reactive substances (TBARS), reduced glutathione (GSH), catalase (CAT), glutathione peroxidase (GSH-Px) and CuZn-SOD levels by spectrophotometric method. The results indicated that although TCDD significantly (p <= 0.01) increased formation of TBARS, it caused a significant decline in the levels of GSH, CAT, GSH-Px and CuZn-SOD in rats. In contrast, curcumin, myrcene and cineole significantly increased GSH, CAT, GSH-Px and CuZn-SOD levels but decreased formation of TBARS. Additionally, the antioxidative effects of curcumin, myrcene and cineole were increased at day 60 compared to day 30. In the TCDD groups given curcumin, myrcene and cineole, oxidative stress decreased by time. In conclusion, curcumin, myrcene and cineole showed antioxidant activity and eliminated TCDD-induced oxidative stress in rats in a time-dependent manner.
Associations between second-trimester amniotic fluid levels of ADAMTS4, ADAMTS5, IL-6, and TNF-? and spontaneous preterm delivery in singleton pregnancies
(Walter De Gruyter Gmbh, 2019) Melekoglu, Rauf; Yilmaz, Ercan; Ciftci, Osman; Kafadar, Yusuf Taner; Celik, Ebru
Background: We investigated the roles of inflammatory cytokines and the A disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS) family in the etiopathogenesis of spontaneous preterm delivery by comparing the ADAMTS4, ADAMTS5, interleukin (IL)-6, and tumor necrosis factor-alpha (TNF-alpha) levels in second-trimester amniotic fluid between pregnant women with preterm birth and term controls. Methods: All pregnant women who underwent second-trimester amniocentesis for genetic analysis between January 1, 2016, and January 1, 2018, were enrolled in this study. From this cohort, 22 patients who subsequently experienced spontaneous preterm delivery before 34 weeks of pregnancy formed the study group, and 22 age- and body mass index (BMI)-matched patients without preterm birth constituted the control group. Results: No significant differences were observed between the preterm birth and control groups in terms of age, BMI, obstetric history of preterm delivery, gestational age at amniocentesis, or indication for amniocentesis. The mean amniotic fluid levels of ADAMTS4 and ADAMTS5 were significantly increased in the preterm birth group compared to the control group (248.3 +/- 22.6 and 182.4 +/- 19.8 pg/mL, P = 0.012; and 198.6 +/- 21.6 and 159.1 +/- 21.7 pg/mL, P = 0.035, respectively). Significantly increased IL-6 and TNF-a levels were also detected in the amniotic fluid of women who experienced spontaneous preterm delivery, relative to controls (142.1 +/- 16.2 and 95.8 +/- 16.4 pg/mL, P < 0.001; and 139.4 +/- 12.5 and 89.6 +/- 11.2 pg/mL, P < 0.001, respectively). Conclusion: The results of this study imply that increased mid-trimester amniotic fluid levels of ADAMTS4, ADAMTS5, IL-6, and TNF-alpha play an important role in the pathophysiology of spontaneous preterm delivery.
Benefical Effects of Beta Glucan Against TCDD Side Effects on The Hepatotoxicity System in Rats
(Wiley, 2018) Ciftci, Osman; Turkmen, Nese Basak; Taslidere, Asli; Gul, Cemile Ceren
[Abstract Not Available]
The beneficial effects of 18?-glycyrrhetinic acid following oxidative and neuronal damage in brain tissue caused by global cerebral ischemia/reperfusion in a C57BL/J6 mouse model
(Springer-Verlag Italia Srl, 2014) Oztanir, M. Namik; Ciftci, Osman; Cetin, Asli; Durak, M. Akif; Basak, Nese; Akyuva, Yener
This study investigated the effects of 18 beta-glycyrrhetinic acid (GA) on neuronal damage in brain tissue caused by global cerebral ischemia/reperfusion (I/R) in C57BL/J6 mice. All subjects (n = 40) were equally divided into four groups: (1) sham-operated (SH), (2) I/R, (3) GA, and (4) GA+I/R. The SH group was used as a control. In the I/R group, the bilateral carotid arteries were clipped for 15 min, and the mice were treated with the vehicle for 10 days. In the GA group, mice were given GA (100 mg/kg) for 10 days following a median incision without carotid occlusion. In the GA+I/R group, the I/R model was applied to the mice exactly as in the I/R group, and they were then treated with the same dose of GA for 10 days. Cerebral I/R significantly induced oxidative stress via an increase in lipid peroxidaitons and a decrease in elements of the antioxidant defense systems. However, GA treatment was protective against the oxidative effects of I/R by inducing significant increases in antioxidant defense systems and a significant decrease of lipid peroxidations. Additionally, cerebral I/R increased the incidence of histopathological damage and apoptosis in brain tissue, but these neurodegenerative effects were eliminated by GA treatment. Therefore, the current study demonstrated that GA treatment effectively prevents oxidative and histological damage in the brain caused by global I/R. In this context, GA may be useful for the attenuation of the negative effects of global cerebral I/R and, in the future, it may be a viable and safe alternative treatment for ischemic stroke in humans.
The beneficial effects of 18?-glycyrrhetinic acid on the experimental autoimmune encephalomyelitis (EAE) in C57BL/6 mouse model
(Taylor & Francis Ltd, 2018) Kamisli, Suat; Ciftci, Osman; Taslidere, Asli; Turkmen, Nese Basak; Ozcan, Cemal
Aim: The aim of this study was to investigate the beneficial effects of 18 beta-glycyrrhetinic acid (GA) on the experimental allergic encephalomyelitis (EAE) in C57BL/6 mice. GA is a natural substance found in the root of licorice and is used in traditional Chinese medicine. It has many pharmacological activities such as antioxidant, anti-inflammatory, and anti-cancer effects. Materials and methods: A total of 40 C57BL/6 mice were divided equally into four groups: (1) Control, (2) EAE, (3) GA and (4) GAthornEAE. 14 days after induction of EAE with MOG35-55 and pertussis toxin, mice were treated with GA at doses of 100 mg/kg/day for 7 days intraperitoneally. Results: To our results, oxidative stress and lipid peroxidations (elevated TBARS levels, decreased GPx, SOD, CAT, and GSH levels) were significantly (p<. 01) increased, causing EAE in brain tissue. Also, histopathological damage (Caspase-3 and IL-17 activity, p <=.01) and cytokine levels (TNF-alpha and IL-1 beta, p<. 01) were induced with EAE in mice brain tissue. On the other hand, GA treatment significantly (p<. 01) reversed oxidative histological and immunological alterations caused by EAE. Conclusions: In conclusion, the GA treatment can protect the brain tissue against EAE in mice with its antioxidant and anti-inflammatory properties.
Beneficial effects of ?-glucan against cisplatin side effects on the nervous system in rats
(Acta Cirurgica Brasileira, 2016) Kaya, Kursat; Ciftci, Osman; Cetin, Asli; Tecellioglu, Mehmet; Basak, Nese
PURPOSE: To investigate the protective effect of Bg on cisplatin (CP)-induced neurotoxicity in rats. METHODS: Twenty eight rats were randomly distributed into four groups. The first group was kept as a control. In the second group, CP was given at the single dose of 7 mg/kg intraperitoneally. In the third group, beta g was orally administered at the dose of 50 mg/kg/day for 14 days. In the fourth group, CP and beta g were given together at the same doses. RESULTS: CP treatment caused significant oxidative damage via induction of lipid peroxidation and reductions antioxidant defense system potency in the brain tissue. In addition, histopathological damage increased with CP treatment. On the other hand, beta g treatment largely prevented oxidative and histopathological negative effects of CP. CONCLUSIONS: Cisplatin has severe neurotoxic effects in rats and ag supplementation has significant beneficial effects against CP toxicity depending on its antioxidant properties. Thus, it appears that Ag might be useful against CP toxicity in patients with cancer in terms of nervous system.
Beneficial effects of curcumin and capsaicin on cyclophosphamide-induced premature ovarian failure in a rat model
(Bmc, 2018) Melekoglu, Rauf; Ciftci, Osman; Eraslan, Sevil; Cetin, Asli; Basak, Nese
Background: In recent years, cancer rates have been rising among reproductive-age women. Thus, chemotherapy exposure has become an important cause of premature ovarian failure (POF). There has been growing interest regarding the preservation and restoration of ovarian function before and after oncological treatment because of the reproductive risk of chemotherapeutics and improved long-term survival of cancer patients. In this study, we sought to analyze the effects of curcumin (CRC) and capsaicin (CPS) on cyclophosphamide-induced POF in a rat model. Methods: POF in rats was induced by intraperitoneal injection of 200 mg/kg cyclophosphamide on day 1 and then 8 mg/kg/day for the following 14 days. After 14 days of cyclophosphamide administration, rats were randomly divided into three groups as follows (n = 10/group): POF, POF + CRC (100 mg/kg/day), and POF + CPS (0.5 mg/kg/day) to determine the effects of CRC and CPS on the cyclophosphamide-induced POF rat model. Biochemical, hormonal, and histopathological evaluations were performed on blood and tissue samples 14 days after the CRC and CPS treatments. Results: Malonaldehyde levels were significantly reduced, and glutathione levels and superoxide dismutase activity were significantly increased, in ovarian tissues in the POF + CRC and POF + CPS groups compared with the POF group. In the POF group, we observed hemorrhage and prominent mononuclear cell infiltration beneath the germinative epithelium, vascular congestion in ovarian stroma, hemorrhage around the corpus luteum, and atresia in ovarian follicles. This histopathological damage was significantly improved by treatment with CRC and CPS. There was a significant reduction in serum follicle-stimulating hormone and luteinizing hormone levels in rats treated with CRC and CPS compared with the POF group. Moreover, the levels of estradiol and anti-mullerian hormone in rats treated with CRC and CPS were significantly increased compared with the control group. Conclusions: In conclusion, CRC and CPS treatment of rats with cyclophosphamide-induced POF had a beneficial effect on reducing ovarian damage by improving tissue oxidative stress marker levels, ovarian reserve marker levels, and histopathological parameters. The significant improvements in ovarian tissue histopathological damage and hormonal levels detected in this study indicate that treatment with CRC or CPS might be a conservative treatment approach for cyclophosphamide-induced POF.
The Beneficial Effects of Fish Oil Following Cisplatin-Induced Oxidative and Histological Damage in Liver of Rats
(Briefland, 2017) Ciftci, Osman; Onat, Elif; Cetin, Asli
This study investigated the protective effect of fish oil (FO) on cisplatin (CP) toxicity in the rat liver. Twenty-eight rats were divided equally into four groups, with the first being a control group. The second group (CP group) was given 7 mg/kg of CP and the third group (FO group) was given 1 FO softgel/rat/day for 14 days. The rats in the fourth group (CP + FO group) were treated with both CP and FO at the above doses. CP treatment caused significant oxidative damage via an increase in thiobarbituric acid reactive substances (TBARS) and reduced antioxidant defenses through a decrease in the activities of catalase (CAT), superoxide dismutase (SOD), reduced glutathione (GSH), and glutathione peroxidase (GPx) in rat liver tissue. Also, CP caused histopathological abnormalities, including necrosis, in the liver tissue. However, concurrent FO treatment prevented the negative oxidative and histopathological effects of CP. In conclusion, CP treatment can cause hepatotoxicity in rats, but dietary supplementation with FO can attenuate the oxidative and histological changes caused by CP. Thus, FO may be useful in preventing CP-induced hepatotoxicity in cancer patients.
The beneficial effects of Montelukast against 2,3,7,8-tetrachlorodibenzo-p-dioxin toxicity in female reproductive system in rats
(Acta Cirurgica Brasileira, 2016) Melekoglu, Rauf; Ciftci, Osman; Cetin, Ash; Basak, Nese; Celik, Ebru
PURPOSE: To determine the toxic effect of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on reproductive system and the beneficial effects of Montelukast (ML) with histological and biochemical analysis. METHODS: Rats were randomly divided into four equal groups (control, TCDD, ML and TCDD+ML). Tissue samples were collected on day 60 and oxidative status and histological alterations were analyzed. RESULTS: The results showed a significant increase in oxidative and histological damage on uterine and ovarian tissues. Otherwise, the oxidative and histological damages caused by TCDD were prevented with ML treatment. CONCLUSION: The toxic effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin on female reproductive system were reversed with Montelukast treatment. Therefore, we claimed that ML treatment might be useful for TCDD toxicity.
The beneficial effects of nerolidol and hesperidin on surgically induced endometriosis in a rat model
(Taylor & Francis Ltd, 2018) Melekoglu, Rauf; Ciftci, Osman; Eraslan, Sevil; Cetin, Asli; Basak, Nese
The objective of this article is to analyze the effects of nerolidol and hesperidin treatment on surgically induced endometriosis in a rat model. Endometriosis was induced in 24 healthy adult female Wistar albino rats via homologous uterine horn transplantation. Three operations were performed on each rat. After the second operation, the rats were randomized into control, nerolidol, and hesperidin treatment groups, and medications were administered for 2 weeks. The effects of the drugs on the endometriotic foci were evaluated after the third operation. Compared with the endometriosis control group, the average volume of the lesions was significantly lower in rats treated with hesperidin and nerolidol. Malondialdehyde levels were significantly reduced in the nerolidol-treated group, and glutathione levels and superoxide dismutase activity were significantly elevated in the endometriotic foci of both the hesperidin- and nerolidol-treated groups compared with the endometriosis group. Hesperidin and nerolidol treatment also improved histological parameters, such as hemorrhage, vascular congestion, necrosis, and inflammatory cell infiltration in the endometriotic foci. The results of this study demonstrated that treatment with the potent antioxidants nerolidol and hesperidin caused a significant regression of surgically induced endometriotic foci in rats.
Beneficial effects of nerolidol on thioacetamide-induced damage of the reproductive system in male rats
(Allied Acad, 2016) Celik, Huseyin; Camtosun, Ahmet; Ciftci, Osman; Cetin, Asli; Aydin, Muhterem; Gurbuz, Sukru
In this study, it was aimed to determinate beneficial effects of Nerolidol (NLR) against reproductive toxicity caused by Thioacetamide (TAA). Male, 3-4-months-old, rats (n=32) were divided into four groups. Group-1 was kept as control and given corn oil as carrier. Group-2 received TAA (200 mg/kg, intraperitoneal (i.p.), two times per week) for 3 weeks, in group-3; NRL was orally administered at the dose of 100 mg/kg per every other day by gavages, group-4; 200 mg/kg TAA and 100 mg/kg NRL were given. Thiobarbituric Acid Reactive Substances (TBARS) and reduced Glutathione (GSH) levels, Catalase (CAT), Superoxide Dismutase (SOD) and Glutathione Peroxidase (GPX), sperm parameters and reproductive organs weight were determined. TAA caused a significant rise in TBARS level and a significant reduce in GPX, CAT, SOD and GSH levels in the testicular tissues compared with the control group, while NLR led to significant reduce in lipid peroxidation via decreasing TBARS level and increasing the levels of GPX, CAT, SOD and GSH. Besides, sperm parameters significantly reduced, and pathologic testicular damage increased with TAA exposure. However, these effects of TAA on sperm parameters and histopathological changes were reversed by NLR treatment. In conclusion, our results demonstrate that the management of TAA induced the testicular damage and NLR prevented thioacetamide-induced testicular damage in rats.
Beta-glucan attenuates cerebral ischemia/reperfusion-induced neuronal injury in a C57BL/J6 mouse model
(Univ Sao Paulo, Conjunto Quimicas, 2019) Kaya, Kursat; Ciftci, Osman; Oztanir, Mustafa Namik; Taslidere, Elif; Turkmen, Nese Basak
Beta-glucans (beta g), that have many useful effects on human health, are natural polysaccharides. Our aim in this study was to determine useful effect of beta g against oxidative and neuronal damage caused by global cerebral ischemia/reperfusion (IR) in stroke imitated mice via surgical operation. A total of 40 mice divided into four equal groups randomly. The group 1 (sham operated) was kept as control. Bilateral carotid arteries of subjects in group 2 (I/R) and group 4 (I/R + beta g) were clipped for 15 min, and the mice in group 4 (I/R + beta g) were treated with beta g (50 mg/kg/day), while the mice in group 2 (I/R) were treated with only vehicle for 10 days. The mice of group 3 (beta g) were treated with beta g for 10 days without carotid occlusion. Global cerebral I/R significantly increased oxidative stress and decreased members of anti-oxidant defense system. In addition, I/R caused histopathological damage in the brain tissue. However, beta g treatment ameliorated both oxidative and histopathological effects of I/R. Our present study showed that beta g treatment significantly ameliorated oxidative and histological damage in the brain tissue caused by cerebral I/R. Therefore, beta g treatment can be used as supportive care for ischemic stroke patients.
Beta-glucan effects on 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) toxicity in liver and brain
(Taylor & Francis Ltd, 2022) Turkmen, Nese Basak; Ozek, Dilan Askin; Taslidere, Asli; Dogan, Fatih; Ciftci, Osman
2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is a common environmental contaminant that is toxic to brain, heart, kidney and liver. TCDD toxicity is due to free radical formation. Beta-glucan is an antioxidant that exhibits beneficial effects on health. We investigated the effects of beta-glucan on brain and liver tissues of rats with TCDD induced toxicity. We used female rats divided into four groups: control, TCDD group treated with TCDD 2 mu g/kg/week, beta-glucan group treated with 50 mg/kg/day beta-glucan for 3 weeks, TCDD + beta-glucan group treated with 2 mu g/kg/week TCDD and 50 mg/kg/day beta-glucan together for 3 weeks. We found that the thiobarbituric acid reactive substance (TBARS) levels were increased significantly in the TCDD group compared to the other groups. Glutathione (GSH) levels, and superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) activities were reduced in the TCDD group compared to the control group. SOD, CAT, GPx activities and GSH levels were increased in the TCDD + beta-glucan group. Histopathological observations were consistent with our biochemical findings. The oxidative stress and histopathology caused by TCDD were ameliorated by beta-glucan treatment. Beta-glucan should be explored for preventing brain and liver damage caused by TCDD toxicity.
Beta-glucan prevents toxic effects of 2,3,7,8-TCDD in terms of oxidative and histopathological damage in heart tissue of rats
(Univ Sao Paulo, Conjunto Quimicas, 2018) Ciftci, Osman; Duman, Ahmet Sefa; Turkmen, Nese Basak; Taslidere, Asli
2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is a widespread environmental contaminant which causes severe toxic effects. Despite there is some suggestion concerning with TCDD induced cardiotoxicity such as formation of free radicals, the main mechanism has not been entirely explained. Beta-glucan is known as strong antioxidant matter and can scavenge free radicals. Therefore this study aimed to investigate the protective effects of beta-glucan against TCDD induced cardiotoxicity in rats. In this study, 2-3 months of age and 190-250 g in weight 32 rats were randomly divided into four equal groups (n=8 for each group). Group 1 was control; Group 2 was TCDD group (2 mu g/kg/week); group 3 was the beta-glucan group(50 mg/kg/day), and group 4 was TCDD and beta-glucan treatment group. The heart samples were taken from rats after 21 days treatment. The results were shown that Despite TCDD exposure visibly caused to increase (p <= 0.001) in TBARS levels, It caused a visible decline in the levels of GSH, CAT, GSH-Px, and SOD. However Beta glucan significantly increased GSH, CAT, GSH-Px, SOD levels and decreased generation of TBARS. Additionally, our histopathological observations were in agreement with the biochemical results. In conclusion, Beta-glucan treatment exhibited protective activity on TCDD induced cardiotoxicity.
Comparison of Reproductive Toxicity Caused by Cisplatin and Novel Platinum-N-Heterocyclic Carbene Complex in Male Rats
(Wiley, 2011) Ciftci, Osman; Beytur, Ali; Cakir, Oguz; Gurbuz, Nevin; Vardi, Nigar
Cisplatin and other platinum complexes are important chemotherapeutic agents and useful in the treatment for several cancers such as prostate, ovarian and testis. However, severe side effects including reproductive toxicity of cisplatin and other platinum complex cause limitations in their clinical usage. In this context, we aimed to compare the damage in testis caused by cisplatin and a novel platinum-N-heterocyclic carbene complex (Pt-NHC). To this end, 35 Sprague-Dawley rats were divided randomly into five equal groups (n = 7 in each group). Cisplatin and Pt-NHC were intraperitoneally administered as a single dose of 5 mg/kg or 10 mg/kg, and the rats were then killed 10 days after this treatment. The testicular tissues and serum samples were taken from all rats for the determination of reproductive toxicity. The results showed that cisplatin and Pt-NHC caused toxicity on the reproductive system via increased oxidative and histological damage, decreased serum testosterone levels and negatively altered sperm characteristics in a dose-dependent manner (p < 0.05). At the same dose levels, cisplatin generally caused lower toxicity on the reproductive system compared with Pt-NHC. In conclusion, these results suggest that Pt-NHC has more toxic effects on the male reproductive system than cisplatin, and in terms of clinical usage, Pt-NHC may be unsafe compared with cisplatin.

Yazar "Ciftci, Osman" seçeneğine göre listele

Sayfa Başına Sonuç

Sıralama seçenekleri